Anti-lipid peroxidation and protection of ginsenosides against cerebral ischemia-reperfusion injuries in rats.
The correlation between protective effect of ginsenosides Rb + R0 and brain endogenously-derived prostacyclin synthesis, thromboxane A2 formation and lipid peroxidation were estimated in rats. Ginsenosides Rb + R0 100 mg/kg iv 30 min before 4-vessel occlusion elevated 6-keto-PGF1 alpha level, declined thromboxane B2 and brain edema formation, reduced the rise of lipid peroxides and suppressed the reduction in both creatine phosphokinase (CK) and superoxide dismutase (SOD) activities in brain tissue after 40-min ischemia followed by 1-h reperfusion. Furthermore, these improvements were partially abolished by pretreating with iv indomethacin. It is concluded that ginsenosides possess protective effect on cerebral ischemia-reperfusion injury of rats and ginsenosides Rb + R0 are the active principles. The underlying mechanism of protection is ascribed partially or mainly to the facilitated synthesis and release of prostacyclin, reduced formation of thromboxane A2 and inhibited generation of free radicals and subsequent lipid peroxidation.
Chu
G X
GX
Department of Pharmacology, Hu-nan Medical University, Changsha, China.
Chen
X
X
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D000818:Animals; D003402:Creatine Kinase / Q000378:metabolism; D005260:Female; D036145:Ginsenosides; D002546:Ischemic Attack, Transient / Q000628:therapy*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D005894:Panax; D010946:Plants, Medicinal; D051381:Rats; D011919:Rats, Inbred Strains; D015427:Reperfusion Injury / Q000517:prevention & control*; D012503:Saponins / Q000627:therapeutic use*; D013482:Superoxide Dismutase / Q000378:metabolism; D013929:Thromboxane B2 / Q000378:metabolism
D036145:Ginsenosides; D012503:Saponins; D008315:Malondialdehyde; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D013482:Superoxide Dismutase; D003402:Creatine Kinase